Renal & Urinary

Front 1

What are the three hormones that the kidneys synthesize and secrete?

Back 1

Renin
Erythropoietin
1,25-dihydroxycholecalciferol

Front 2

What are the causes for transitional cell carcinoma of the bladder?

Back 2

1. smoking cigarettes (most common cause)
2. workers in dye, rubber, or leather industries
3. cyclophosphamide
4. arsenic exposure
5. beer consumption (due to nitrosamines in beer)
6. schistsoma hematobium (70% squamous cell, 30% transitional)

Front 3

What are reasons for metabolic acidosis with a normal anion gap?

Back 3

diarrhea
glue sniffing
renal tubular acidosis
hyperchloremia

Front 4

What is the corresponding electrolyte abnormality with low and high Na?

Back 4

low: disorientation, stupor, coma
high: neurological – irritability, delirium, coma

Front 5

What is the corresponding electrolyte abnormality with low and high Cl?

Back 5

low: secondary to metabolic alkalosis, hypokalemia, hypovolemia, increased aldosterone
high: secondary to non-anion gap acidosis

Front 6

What is the corresponding electrolyte abnormality with low and high K?

Back 6

low: U waves on EKG, flattened T waves, arrhythmias, paralysis
high: peaked T waves, wide QRS, arrhythmias

Front 7

What is the corresponding electrolyte abnormality with low and high Ca?

Back 7

low: tetany, neuromuscular irritability
high: delirium, renal stones, abdominal pain, not necessarily calciuria

Front 8

What is the corresponding electrolyte abnormality with low and high Mg?

Back 8

low: neuromuscular irritability, arrhythmias
high: delirium, decreased DTRs, cardiopulmonary arrest

Front 9

What is the corresponding electrolyte abnormality with low and high PO4?

Back 9

low: low-mineral ion product causes bone loss, osteomalacia
high: high-mineral ion product causes renal stones

Front 10

In which glomerular disease would you expect to see the following changes?
(a) foot process effacement (EM)
(b) wire-loop appearance (LM)
(c) mesangial deposits of IgA (EM)
(d) crescent-moon shaped lesion (LM)
(e) segmental sclerosis and hyalinosis (LM)

Back 10

a) minimal change disease
b) diffuse proliferative GN
c) Berger's
d) RPGN
e) focal segmental

Front 11

What constitutes a nephritic syndrome? Examples?

Back 11

(a) inflammatory process
(b) when it involves golmeruli, it leads to hematuria and RBC casts in urine
(c) associated with azotemia, oliguria, hypertension, and proteinuria (<3.5 g/day)
i. acute poststeptococcal
ii. rapidly progressive (crescentic) glomerulonephritis
iii. diffuse proliferative glomerulonephritis (due to SLE or MPGN)
iv. Berger's disease (IgA glomerulanephropathy)
v. Alport's Syndrome

Front 12

What constitutes a nephrotric syndrome? Examples?

Back 12

(a) massive proteinuria (>3.5g/day)
(b) hyperlipidemia, fatty casts, edema
(c) associated with thromboembolism and increased risk of infection
i. membranous glomerulonephritis (diffuse membranous)
ii. minimal change (lipoid nephrosis)
iii. amyloidosis
iv. diabetic glomerulonephropathy
v. focal segmental glomerulosclerosis
vi. membranoproliferative glomerulonephritis

Front 13

Wire loop appearance on LM

Back 13

diffuse proliferative GN

Front 14

mesangial deposits of IgA on Em

Back 14

Berger's dissease

Front 15

In which glomerular disease do we see Kimmeslstiel-Wilson lesions on LM? (sclerosed nodules)

Back 15

Diabetic nephroglomeropathy

Front 16

In which glomerular disease do we see "spike and dome" appearance on EM?

Back 16

Membranous glomerulonephritis

Front 17

In which glomerular disease do we see "tram track"ing of subendothelial humps (EM)?

Back 17

Membranoproliferative glomerulonephritis

Front 18

In which glomerular disease do we see subepithelial humps (EM)?

Back 18

post-strep glomerulonephritis

Front 19

What is the WAGR complex?

Back 19

(a) Wilm's Tumor – most common renal malignancy of early childhood (ages 2-4), contrain embryonic glomerular structures. Presents with huge, palpable flank mass and/or hematuria
(b) deletion of tumor suppresor gene WT1 on chromosome 11, may be part of WAGR complex
i. Wilm's Tumor
ii. Aniridia
iii. Genitourinary malformations
iv. Retardation (mental-motor)

Front 20

What side effects are common with ACE inhibitor administration?

Back 20

(a) Coughing (caused to bradykinin inactivation)
(b) Angioedema
(c) Proteinuria
(d) Taste changes
(e) HypOtension
(f) Pregnancy problems (fetal renal damage)
(g) Rash
(h) Increased renin
(i) Lower AII

Front 21

In cases of hyperkalemia, what can be done to acutely shit K out of the serum and into the cells in order to avoid cardiac arrhythmias?

Back 21

Insulin
b-agonists

Front 22

Why do the kidneys retain fluid in heart failure patients?

Back 22

CHF = decreased EF, leading to slower CO, sensed as decrease in fluid

activation of renin-angiotensin-aldosterone system

Front 23

In which glomerular disease do we see anti-GBM antibodies on IF?

Back 23

Goodpasture's (one of the RPGNs)
-- crescentic
also includes Wegener's (w/c-ANCA)
pauci (p-ANCA)

Front 24

Describe circulation through the liver, kidneys, and heart.

Back 24

Liver -- largest sgare if systemic CO

Kidney -- highest blood flow per gram of tissue

Heart -- large arteriovenous O2 difference b/c O2 extraction is always 100%. Increased O2 demand is met by increased coronary blood flow, not increased extraction of O2.

Front 25

How do NSAIDs cause renal damage?

Back 25

Prostaglandins dilate afferent arterioles (leading to increased RPF and GFR) – NSAIDs inhibit this process. This will keep the RPF low, and in this scenario, his creatinine is high, suggesting that he has kidney failure. In the situation, his JG cells (modified smooth muscles of afferent arteriole) and macula densa (Na sensor, part of distal convoluted tubule) sense the decreased renal perfusion and secrete renin in response. Angiotensin II is already constricting the afferent arteriole in addition to the efferent one.

Front 26

When is ANP released? What effect does it have in the kidney?

Back 26

ANP is released from the atria in reponse to increased BV and atrial pressure. Causes generalized vascular relaxation. Constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated), promoting diuresis and contributing to the "escape from aldosterone" mechanism.

Front 27

How is renal clearance calculated?

Back 27

Cl = UV/P

if Cl < GFR = reabsorption
if Cl > GFR = secretion
if Cl = GFR, neither secretion nor reabsorption

Front 28

In terms of fluctuations in BP, which receptors detect what?

Back 28

1. aortic arch transmits via vagus nerve to medulla (responds ONLY to increased BP)

2. carotid sinus transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to decrease and and increased in BP)

Front 29

What do the following Q waves suggest?

1. V1 - V4
2. V1 - V2
3. V4 - V6
4. I, aVL
5. II, III, aVF

Back 29

1. anterior wall (LAD)

2. anteroseptal (LAD)

3. anterolateral (LCX)

4. lateral wall (LCX)

5. inferior wall (RCA)

Front 30

How is GFR calculated?

Back 30

GFR = Kf [(Pgc - Pbs) - (pigc - pibc)

pibs normally = 0

Front 31

How do nitrates affect

EDV
BP
contractility
heart rate
ejection time
myocardial oxygen consumption

Back 31

decreased EDV, BP, ejection time, MVO2

reflexive increase in contractility and heart rate

Front 32

What is the Cushing reaction? What is responsible?

Back 32

Increased intracranial pressure constricts arterioles, which leads to cerebral brain ischemia, leading to hypertension. Sympathetic response --> reflex bradycardia.

Cushing triad = hypertension, bradycardia, respiratory depression.

Front 33

How do b-blockers affect

EDV
BP
contractility
heart rate
ejection time
myocardial oxygen consumption

Back 33

increased EDV (b/c of vasocontriction) and ejection time

decreased BP, contractility, heart rate, MVO2

nifedipien is similar to nitrates in effect; verapamil is similar to b-blockers in effect.

partial b-agonists are contraindicated in angina (pindolol, acebutolol)

Front 34

How does creatinine clearance relate to GFR?

Back 34

apprx measure -- slightly overestimates GFR b/c creatinine is moderately secreted by the renal tubules

Front 35

What is nephrotic syndrome caused by?

Back 35

damage to the glomerulus, causing increased filtration of serum protein. Podocytes dysfunctional

Front 36

What does the early PT absorb?

Back 36

most of Na, H20, bicard, glucose, aa, phosphate, lactate, Mg, Ca

Front 37

What does the TAL reabsorb?

Back 37

Na
Mg (Ca competes. hypercalcemia leads to Mg excretion)

Front 38

Where does ADH eork?

Back 38

late CD -- principal cells

Front 39

Differentiate principal and a-intercalated cells in DT/CD?

Back 39

principal -- resorb Na, H2O, secrete K

intercalated -- secrete H+, resorb K via H+,K+ ATPase

Front 40

What are the methods of autoregulation in the kidney?

Back 40

1. myogenic -- afferent contract in response to stretch

2. tubuloglomerular feedback -- increased renal artieral pressure = increased delivery to macula densa, which will constrict afferent arteriole

Front 41

What substance can be used to measure RPF? What are its characteristics?

Back 41

PAH is filtered and secreted by renal tubules, underestimates by 10% (does not fully perfuse kidney)

Front 42

What is prerenal azotemia? What are examples?

Back 42

azotemia = increased levels of creatinine, BUN

BUN:CRE > 20:1
e.g. making a shit-ton of urea (waste), not filtering

hypoperfusion (hemorrhage, shock)
volume depletion
CHF
renal artery stenosis

Front 43

What is the normal FF (GFR/RPF)

Back 43

FF = 20%

80% leaves efferent --> peritubular capillary circulation

Front 44

What is the governing for of GFR?

Back 44

P(bs), which increases with afferent dilation and efferent constriction

Front 45

What happens to GFR and RPF when the ureters are constricted? Increased in protein concentration?

Back 45

1. P(bs) increases, leading to decreased GFR

2. Pi(gs) increases, leading to decreased GFR.

Front 46

Histologically, what is seen in Wilms' tumor? What does tumor suppressor gene WT1 regulate?

Back 46

Tumor tends to recapitulate different stages of embryological formation of the kidney, so that three classic histological areas are described: a stromal area, a blastemal aera of tightly packed embryonic cells, and a tubular area.

WT1 regulated the outgrowth of the uteric bud from the mesonephros.

Front 47

describe glucose clearance in relation to threshold.

Back 47

glucose at a normal plasma level is completely reabsorbed in the PT by Na/glucose cotransport.

At plasma glucose of 1160 - 200 mg/dL, glucosuria begins (threshold). At 350 mg/dL, all transporters are fully saturated.

Front 48

Where in the kidney does PTH affect? AII?

Back 48

early PT, inhibits Na/phosphate co-tranport --> phosphate excretion;
early DT -- increase Ca/Na exchange = Ca reabsorption

early PT, stimulates Na/H exchange --> increased Na and H2O reabsorption

Front 49

Where does aldoesterone take effect?

Back 49

in principal cell of CT -- leads to insertion of Na channel on luminal side, resorbing Na in exchange for secretion of K and H

Front 50

Where does ADH take effect in the kidney?

Back 50

acts as V2 receptors --> insertion of aquaporin H2O channels on luminal side

Front 51

What is Fanconi Syndrome?

Back 51

heavy metal poisoning. PTC undergoes coagulation necrosis, cannot absorb ANYTHING.

Front 52

What is Barter's Syndrome?

Back 52

majority in children
renal defct in Cl reabsorption in Na/K/2Cl cotransporter -- loss of ions in urine; leads to augmented exchange of Na and excretion of K in distal/collecting tbules (causes hypokalemia and metabolic acidosis)

- normotensive b/c of vasodilation
- muscle weakness (hypokalemia)
- increased renin

Front 53

How does hypokalemia affect the kidneys?

Back 53

increases prostaglandin syn in kidneys, stimulates hyperplasia og JXG apparatus, increased renin = hyperaldosteronism

Front 54

What does TF/P mean?

Back 54

[tubular fluid]/[plasma}

when TB/P > 1, solute is either reabsorbed less quickly than water or there is net secretion of solute

when TB = 1, solute and water are reabsorbed at the same rate

when TB < 1, solute is reabsorbed more quickly than water

Front 55

As it travels down the PT, what happens to the TF/P of the following?

1. PAH
2. creatinine
3. inulin
4. urea, Cl
5. K, Na
6. bicarb, aa, glucose

Back 55

1. PAH is secreted, so > 1

2,3. tubular cretinine and inuline increase in concentration due to water reabsorption, not secretion

4. Cl reabsorption occurs at a slower rate than Na in proximal 1./3 of the PT and then matches the rate of Na reabsorption more ditally. Thus, its relative concentration increases before it plateaus.

5. Na reabsorption drives H20 resaborption, so it matches on = 1

6. absorbed very quickly < 1

Front 56

How does ACE inhibitor work on the kidney?

Back 56

AII preferntially constricts efferent arteriold. ACE inhibits this vasoconstriction.

Front 57

What is the path of blood filtration through the kidney?

Back 57

renal artery
segmental
lobar
arcuate
afferent
glomerulus
efferent
vasa recta
segmental vein
renal vein

Front 58

What is the function of the JGA?

Back 58

(modified smooth muscle of afferent arteriole) and macula densa (Na sensor, part of the distal convoluted tubule).

JG cells secrete renin in response to decreased renal BP, decreased Na delivery to distal tubule, and increased sympathetic tone

Front 59

How can high insulin levels lead to hypertension?

Back 59

because insulin:
1. Enhances sodium reabsorption in the kidneys
2. Stimulates the sympathetic nervous system by activating sympathetic centers in the brain
3. Increases the pressor response to angiotensin II
4. Increases angiontensin II production
5. Increases sodium sensitivity
6. Stimulates smooth muscle proliferation
7. increased intracellular Ca2+

Front 60

What shifts K out of the cell (causing hyperkalemia)?

Back 60

1. insulin deficiency (decreased Na/K ATPase)
2. b blockers (decreased Na/K-ATPase)
3. acidosis, extreme exercise (increase K/H exchange)
4. hyperosmolarily
5. digitalis (blocks Na/K-ATPase)
6. cell lysis
7. renal failure, interstial nephritis

Front 61

What shifts K into the cell (causing hypokalemia)?

Back 61

1. insulin (increases Na.K-ATase)
2. b agonist
3. alkalosis
4. hypo-osmolarity

Front 62

What is Henderson-Hasselbalch equation?

Back 62

pH = pKa + [HCO3]/(0.03 Pco2)

Front 63

How can respiratory compensation in response to metabolic acidosis can be quantified?

Back 63

Pco2 = 1.5 (HCO) + 8H

Front 64

How can respiratory compensation to metabolic alkalosis be quantified?

Back 64

7mmHg for each 1 mEq/L rise in HCO3

Front 65

How can renal compensation to chronic respiratory acidosis/alkalosis be quantified?

Back 65

HCO3 = (0.4)(increase/decrease in Pco2)

Front 66

What is RTA 1? Etiology?

Back 66

Dital

defect in CT's ability to excrete H+, can't regenerate HCO3 in H/K-ATPase pump.

A/w hypokalamia and risk for Ca-containing kidney stones.

Can be caused by AmpB, light chains in MM

Front 67

What is RTA 2? Etiology?

Back 67

Proximal

defent in PT HCO3 reabsorption. a/w hypoklamemia and hypophosphatemia rickets, osteopetrosis, Fanconi's anemia.

Front 68

What is RTA 4? Etiology?

Back 68

Hyperkalemic

hypoaldosteronism or lack of CT response to aldosterone, destruction of JXG. a/w hyperkalemia and inhibition og ammonium excretion in PT. leads to decreased urine pH due to decreased buffering capacity.

Front 69

What do RBC casts suggest?

Back 69

glomerulonephritis
ischemia
malignant hypertension

Front 70

What do WBC casts suggest?

Back 70

tubulointerstiail inflammation
acute pyleonephritis
transplant rejection

Front 71

What do granular (muddy brown) casts suggest?

Back 71

ATN

Front 72

What do waxy casts suggest?

Back 72

advanced renal disease/CRF

Front 73

What do hyaline casts suggest?

Back 73

nonspecific

Front 74

Are casts seen in bladder cancer, kidney stones, or acute cystitis?

Back 74

No.

Bladder cancer, kidney stones --> hematuria, no casts

Acute cystitis --> pyuria, no casts

Front 75

What does "proliferative" imply in glomerular disorders?

Back 75

Hypercellular glomeruli

Front 76

What does "membranous" imply in glomerular disorders?

Back 76

thicking of the glomerular membrane

Front 77

What are the nephritic syndromes?

Back 77

Acute strep
RPGN (crescentic)
diffuse proliferative GN
Berger's
Alport's

Front 78

What are the nephrotic syndromes?

Back 78

membranous
minimal change
amyloidosis
diabetic GN
focal segmental
membranoproliferative

Front 79

When are oxalate stones seen in the kidney?

Back 79

ethylene glycol or vit C abuse

Front 80

What are ammonium magnesium phosphate stones?

Back 80

Caused by infection with urease-pos bugs (proteus, staph, klebsiella).

Form staghorn calculi.

Front 81

What are cystine stones?

Back 81

Most often secondary to cystinuria. Hexagonal. Treat with alkalinization of urine.

Front 82

Where is RCC commonly found? In whom is it most common? What is seen? How does it present? How does it spread?

Back 82

Commonly gounf as large, solitary yellow mass in upper poles as polygonal clear cells (originates in renal tubular cells). Most common in men 0 - 70.

Increased incidence with smoking and obesity; menifestw tih hematuria, palpable mass, fever and weight loss.

s/w paraneoplastic (epo, ACTH, PTHrP, and prolactin)

Invades IVC and spreads hematog (mets to lung and bone)

a/w with vHL ch 3

Front 83

What is Beckwith Widemann syndrome?

Back 83

Increased risk of childhood cancers (e.g. RCC, neuroblastoma, Wilm's tumor) along with congenital abnormailities (e.g. macroglossia, hemihypertrophy, umbilical hernia, ompalocoaele, ear creases)

Front 84

What is TCC? Found where? Presentation?

Back 84

most common tumor of uts (can occur in renal calycesm renal pelvis, ureters, and bladder)

painless hematuria suggests bladder cander

Front 85

What is urate nephropathy?

Back 85

due to deposition of urate crystals (2ndary to leukemia treatment, lead poisoning, gout) in rental tubules and interstitium; may produce acute renal failure

Front 86

What is drug induced interstitial nephritis? How does it present?

Back 86

Acute insterstitial inflammation. Pyuria (eosinophils) and azotemia occurring 1-2 weeks after administration of drugs (NSAIDs, diuretics, methicillin, sulfonamides, rifampin), which act as hapten, inducing hypersensitiviey

a/w fever, rash, hematuria, CVA tenderness

may cause papillary necrosis, hypertension, chromic renal failure, TCC of bladder and renal pelvis

Front 87

When can diffuse cortical necrosis happen?

Back 87

Acute generalized cortical infarction of both kidneys. Likely due to a combination of vasospasm and DIC.

a.w OB catastrophe's (e.g. abrupto placentae) and septic shock

Front 88

What is ischemic ATN? What is most affected? What are the stages? What are they key?

Back 88

most common -- hemorrhage, vasoconstriction, hypotension, dehydration, shock, sepsis, crush injury (myoglobinuria)

most common cause of acute renal failure in hostpial. self-reversible, but fatal if left untreated. Death most odten occurs during initial oliguric phase.

3 stages: inciting event --> maintenance (low urine output) --> recovery (2-3 weeks)

key findingL granular muddy brown casts

need dialysis

Front 89

What are causes for nephrotoxic ATN?

Back 89

drugs (methacillin, gentamicin, sulfonamides)
radiographic contrast agents
heavy metals
organic solvents
ethylene glycol
myoglobin

Front 90

What is renal azotemia?

Back 90

generally due to ATN or ischemia/toxinds; less common RPGN. patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule --> decreased GFR
BUN reabsorption impaired, so decreased BUN/cre ratio < 15

Front 91

What is postrenal azotemia?

Back 91

due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction

BUN:cre >15

Front 92

What are reasons for renal papillary necrosis?

Back 92

may be triggered by a recent infection or immune stimulus

a/w

diabetes mellitus
acute pyelonephritis
chronic phenacetin use
sickle cell anemia

Front 93

What is the mech and clinical use of mannitol?

Back 93

mech -- osmotic diuretic = increased urine flow

used for shock, drug oversose, increased intracranial/ocular pressure

Front 94

What is the tox of mannitol?

Back 94

Pulmonary edema
dehydration

Front 95

What is the mech, clinical use, and tox and acetazolamiide?

Back 95

carbonic anydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body HCO stores.

use -- glaucoma, urinary alkalinzation, metabolic acidosis, alititude sickness

tox -- hyperchloremic metabolic acidosis, neuropathy, NH3 tox, sulfa allergy

Front 96

What is the mech, clinical use, and tox of furosemide?

Back 96

Sulfonamide loop diurectic. Inhibits NA/K/2Cl of TAL. prevents concentration of urine. increase Ca excretion.

use -- edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia

tox -- ototoxicity, hypokalemia, dehydration, allergy, interstitial nephritis, gout

Front 97

What is the mech, clinical use, and tox of ethacrynic acid?

Back 97

phenozyacetic acid derv, works like furosemide; for those with sulfa allergies

can cause hyperuricemia, acute gout

Front 98

What is the mech, clinical use, and tox of thiazies?

Back 98

inhibits NaCl resborption in DT, reducing diluating capacit of nephron. decreased Ca eccretion

use -- hypertension, CHF, idiopathic hpercalciuria, nephrogenic diabetes insipidus

tox -- hypokalemic metabolic alkalosis, hypoatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia.sulfa allergy

Front 99

What are ACE inhibitors? How do they work?

Back 99

inhibit AII, prevent inactivation of bradykinin, a potent vasodilator. reninn release is increased due to loss of feedback inhibition.

use -- hypertension, CHF, diabetic renal disease

tox --
Cough
Angioedema
Taste changes
hypOtension
fetal renal damage
Rash
Increased renin
Lower angiotenin
Hyperkalemia

Front 100

Why are ACE inhibitors contraindicated in bilateral renal artery stenosis?

Back 100

ACE inhibitors significantly decreased GFR by preventing constriction of efferent arterioles.

In renal artery stenosis, The decreased perfusion pressure (caused by the stenosis) leads to decreased blood flow (hypoperfusion) to the kidney and a decrease in the GFR. If the stenosis is longstanding and severe the GFR in the affected kidneys never increases again and (prerenal) renal failure is the result.